Caenorhabditis elegans: a model organism in Biology

WormBook: Introduction

Caenorhabditis elegans is a small roundworm usually found in soil that often feeds on bacteria among rotting vegetation and decaying organic matter; it is nonparasitic and nonpathogenic. Despite being a primitive invertebrate, C. elegans possesses many of the anatomical features and organs found in higher-level animals, especially pertaining to its nervous, reproductive, muscular, and digestive systems. Because C. elegans is transparent, easily observed and manipulated, has a short life cycle (2–3 weeks), and can be cultivated in large numbers under laboratory conditions, researchers frequently use it to study questions that would be difficult to explore directly in humans and other animals. In particular, because the cells of C. elegans hold steady in number and position in the body throughout its life, it is a popular model organism in developmental biology, embryology, genetics, and neuroscience (AccessScience).

Featured articles (these articles have been added to Science Primary Literature; search this database for more information about C elegans):

*Douglas, A. E. (2019). Simple animal models for microbiome research. Nature Reviews. Microbiology, 17(12), 764-775. [PDF] [Cited by]

The health and fitness of animals, including humans, are influenced by the presence and composition of resident microbial communities. The development of rational microbial therapies to alleviate chronic immunological, metabolic and neurobiological diseases requires an understanding of the processes underlying microbial community assembly and the mechanisms by which microorganisms influence host traits. For fundamental discovery, simple animal models (that is, lower vertebrate and invertebrate species with low diversity microbiomes) are more cost-effective and time-efficient than mammal models, especially for complex experimental designs and sophisticated genetic screens. Recent research on these simple models demonstrates how microbiome composition is shaped by the interplay between host controls, mediated largely via immune effectors, inter-microorganism competition, and neutral processes of passive dispersal and ecological drift. Parallel research on microbiome-dependent host traits has identified how specific metabolites and proteins released from microorganisms can shape host immune responsiveness, ameliorate metabolic dysfunction and influence behavioural traits. In this Review, the opportunity for microbiome research on the traditional biomedical models zebrafish, Drosophila melanogaster and Caenorhabditis elegans, which command superb research resources and tools, is discussed. Other systems, for example, hydra, squid and the honeybee, are valuable alternative models to address specific questions.”

*Jung, Y., Kwon, S., Ham, S., Lee, D., Park, H. H., Yamaoka, Y., Jeong, D., Artan, M., Altintas, O., Park, S., Hwang, W., Lee, Y., Son, H. G., An, S. W. A., Kim, E. J. E., Seo, M., & Lee, S. V. (2020). Caenorhabditis elegans Lipin 1 moderates the lifespan-shortening effects of dietary glucose by maintaining ω-6 polyunsaturated fatty acids. Aging Cell, 19(6), e13150. [PDF] [Cited by]

Excessive glucose causes various diseases and decreases lifespan by altering metabolic processes, but underlying mechanisms remain incompletely understood. Here, we show that Lipin 1/LPIN-1, a phosphatidic acid phosphatase and a putative transcriptional coregulator, prevents life-shortening effects of dietary glucose on Caenorhabditis elegans. We found that depletion of lpin-1 decreased overall lipid levels, despite increasing the expression of genes that promote fat synthesis and desaturation, and downregulation of lipolysis. We then showed that knockdown of lpin-1 altered the composition of various fatty acids in the opposite direction of dietary glucose. In particular, the levels of two ω-6 polyunsaturated fatty acids (PUFAs), linoleic acid and arachidonic acid, were increased by knockdown of lpin-1 but decreased by glucose feeding. Importantly, these ω-6 PUFAs attenuated the short lifespan of glucose-fed lpin-1-inhibited animals. Thus, the production of ω-6 PUFAs is crucial for protecting animals from living very short under glucose-rich conditions.

*Leung, M. C. K., Williams, P. L., Benedetto, A., Au, C., Helmcke, K. J., Aschner, M., & Meyer, J. N. (2008). Caenorhabditis elegans: An Emerging Model in Biomedical and Environmental Toxicology. Toxicological Sciences, 106(1), 5-28. [PDF] [Cited by]

“The nematode Caenorhabditis elegans has emerged as an important animal model in various fields including neurobiology, developmental biology, and genetics. Characteristics of this animal model that have contributed to its success include its genetic manipulability, invariant and fully described developmental program, well-characterized genome, ease of maintenance, short and prolific life cycle, and small body size. These same features have led to an increasing use of C. elegans in toxicology, both for mechanistic studies and high-throughput screening approaches. We describe some of the research that has been carried out in the areas of neurotoxicology, genetic toxicology, and environmental toxicology, as well as high-throughput experiments with C. elegans including genome-wide screening for molecular targets of toxicity and rapid toxicity assessment for new chemicals. We argue for an increased role for C. elegans in complementing other model systems in toxicological research.”

*Schulz, T. J., Zarse, K., Voigt, A., Urban, N., Birringer, M., & Ristow, M. (2007). Glucose restriction extends Caenorhabditis elegans life span by inducing mitochondrial respiration and increasing oxidative stress. Cell Metabolism, 6(4), 280-293. [Cited by]

Increasing cellular glucose uptake is a fundamental concept in treatment of type 2 diabetes, whereas nutritive calorie restriction increases life expectancy. We show here that increased glucose availability decreases Caenorhabditis elegans life span, while impaired glucose metabolism extends life expectancy by inducing mitochondrial respiration. The histone deacetylase Sir2.1 is found here to be dispensable for this phenotype, whereas disruption of aak-2, a homolog of AMP-dependent kinase (AMPK), abolishes extension of life span due to impaired glycolysis. Reduced glucose availability promotes formation of reactive oxygen species (ROS), induces catalase activity, and increases oxidative stress resistance and survival rates, altogether providing direct evidence for a hitherto hypothetical concept named mitochondrial hormesis or “mitohormesis.” Accordingly, treatment of nematodes with different antioxidants and vitamins prevents extension of life span. In summary, these data indicate that glucose restriction promotes mitochondrial metabolism, causing increased ROS formation and cumulating in hormetic extension of life span, questioning current treatments of type 2 diabetes as well as the widespread use of antioxidant supplements.”

*Shen, P., Yue, Y., & Park, Y. (2018). A living model for obesity and aging research: Caenorhabditis elegans. Critical Reviews in Food Science and Nutrition, 58(5), 741-754. [Cited by]

Caenorhabditis elegans (C. elegans) is a free-living nematode that has been extensively utilized as an animal model for research involving aging and neurodegenerative diseases, like Alzheimer’s and Parkinson’s, etc. Compared with traditional animal models, this small nematode possesses many benefits, such as small body size, short lifespan, completely sequenced genome, and more than 65% of the genes associated with human disease. All these characteristics make this organism an ideal living system for obesity and aging studies. This review gives a brief introduction of C. elegans as an animal model, highlights some advantages of research using this model and describes methods to evaluate the effect of treatments on obesity and aging of this organism.

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